Alcohol dependence promotes systemic IFN-γ and IL-17 responses in mice

• Published in: PloS one 2020-12, Vol.15 (12), p.e0239246
• Main Authors: Frank, Kayla, Abeynaike, Shawn, Nikzad, Rana, Patel, Reesha R, Roberts, Amanda J, Roberto, Marisa, Paust, Silke
• Format: Article
• Language: English
• Subjects: Alcoholism; Alcoholism - metabolism; Alcohols; Animals; Antibodies; Biology and Life Sciences; Cytokines; Cytokines - metabolism; Dendritic cells; Dependence; Drug dependence; Ethanol; Ethanol - adverse effects; Exposure; Flow cytometry; Health risks; Immune system; Immunology; Infections; Inflammation; Interferon-gamma - metabolism; Interleukin 10; Interleukin 12; Interleukin 17; Interleukin 4; Interleukin-17 - metabolism; Laboratory animals; Leukocytes (neutrophilic); Liver; Liver - drug effects; Liver - metabolism; Lymphocytes; Lymphocytes B; Male; Medicine and Health Sciences; Mice; Neutrophils; Physical Sciences; Physiological effects; Risk analysis; Risk factors; Social Sciences; Spleen; Spleen - drug effects; Spleen - metabolism; Stability; γ-Interferon
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0239246

Alcohol use disorder (AUD) is a chronic relapsing disorder characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences. AUD is associated with a variety of physiological changes and is a substantial risk factor for numerous diseases. We aimed to characterize systemic alterations in immune responses using a well-established mouse model of chronic intermittent alcohol exposure to induce alcohol dependence. We exposed mice to chronic intermittent ethanol vapor for 4 weeks and analyzed the expression of cytokines IFN-γ, IL-4, IL-10, IL-12 and IL-17 by different immune cells in the blood, spleen and liver of alcohol dependent and non-dependent control mice through multiparametric flow cytometry. We found increases in IFN-γ and IL-17 expression in a cell type- and organ-specific manner. Often, B cells and neutrophils were primary contributors to increased IFN-γ and IL-17 levels while other cell types played a secondary role. We conclude that chronic alcohol exposure promotes systemic pro-inflammatory IFN-γ and IL-17 responses in mice. These responses are likely important in the development of alcohol-related diseases, but further characterization is necessary to understand the initiation and effects of systemic inflammatory responses to chronic alcohol exposure.